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Journal of Cereal Science xxx (2013) 1e7
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Journal of Cereal Science
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Review
Does wheat make us fat and sick?
Fred J.P.H. Brouns a, *, Vincent J. van Buul a, Peter R. Shewry b
a
Maastricht University, Faculty of Health, Medicine and Life Sciences, Department of Human Biology, Health Food Innovation Management, P.O. Box 616,
6200 MD Maastricht, The Netherlands
b
Rothamsted Research, Plant Biology and Crop Science, West Common, Harpenden, Hertfordshire AL5 2JQ, United Kingdom
a r t i c l e i n f o
a b s t r a c t
Article history:
Received 5 February 2013
Received in revised form
27 May 2013
Accepted 3 June 2013
After earlier debates on the role of fat, high fructose corn syrup, and added sugar in the aetiology of
obesity, it has recently been suggested that wheat consumption is involved. Suggestions have been made
that wheat consumption has adverse effects on health by mechanisms related to addiction and overeating. We discuss these arguments and conclude that they cannot be substantiated. Moreover, we
conclude that assigning the cause of obesity to one specific type of food or food component, rather than
overconsumption and inactive lifestyle in general, is not correct. In fact, foods containing whole-wheat,
which have been prepared in customary ways (such as baked or extruded), and eaten in recommended
amounts, have been associated with significant reductions in risks for type 2 diabetes, heart disease, and
a more favourable long term weight management. Nevertheless, individuals that have a genetic
predisposition for developing celiac disease, or who are sensitive or allergic to wheat proteins, will
benefit from avoiding wheat and other cereals that contain proteins related to gluten, including primitive
wheat species (einkorn, emmer, spelt) and varieties, rye and barley. It is therefore important for these
individuals that the food industry should develop a much wider spectrum of foods, based on crops that
do not contain proteins related to gluten, such as teff, amaranth, oat, quinoa, and chia. Based on the
available evidence, we conclude that whole-wheat consumption cannot be linked to increased prevalence of obesity in the general population.
Ó 2013 Published by Elsevier Ltd.
Keywords:
Whole-wheat
Risk-benefit
Gluten-free diet
Celiac disease
1. Introduction
Wheat is the most widely cultivated cereal grain worldwide,
being grown in temperate climates from Scandinavia in the north to
Argentina in the south, including upland regions in the tropics. It is
third among the cereals, behind maize and rice, in total global
production, which was 704 million tons in 2011. The demand for
wheat for human consumption is also increasing globally, including
in countries which are climatically unsuited for wheat production,
due to the adoption of western-style diets. Wheat is relatively rich
in micronutrients, including minerals and B vitamins, and supplies
up to 20% of the energy intake of the global population (Cummins
and Roberts-Thomson, 2009).
About 95% of the wheat that is grown and consumed globally is
bread wheat (Triticum aestivum). Bread wheat is a relatively new
Abbreviations: ATIs, amylase-trypsin inhibitors; CD, celiac disease; GI, glycemic
index; IBS, irritable bowel syndrome.
* Corresponding author. Tel.: þ31 (0) 433 88 14 66; fax: þ31 (0) 433 67 09 76.
E-mail addresses: [email protected] (F.J.P.H. Brouns),
[email protected] (V.J. van Buul), [email protected]
(P.R. Shewry).
species, having arisen in southeast Turkey about 9000 years ago
(Feldman and Millet, 2001). It is hexaploid with three related genomes (termed A, B and D) and probably arose by spontaneous
hybridization between a cultivated form of tetraploid wheat (Triticum turgidum) and a related wild grass species (goat grass, Aegilops tauschii). Most of the remaining 5% of the wheat crop is
tetraploid durum wheat (also called pasta wheat) (T. turgidum var
durum) which is more adapted to the dry Mediterranean climate.
However, small amounts of “primitive” wheats are also grown,
mainly for specialist health foods: einkorn (diploid Triticum monococcum), emmer (tetraploid T. turgidum var dicoccon) and spelt
(hexaploid T. aestivum var spelta). The latter essentially differs from
bread wheat in that the hull is not removed by threshing; resulting
in a higher fibre content when consumed as whole grain.
Although wheat is a young species, it is immensely diverse, with
forms adapted to a wide range of local environments and selected
for different end uses. Feldman et al. (1995) estimated that at least
25,000 genetically distinct forms occur, but this is undoubtedly an
underestimate with previously unreported diversity being
described in recent years in countries such as China. Determination
of the full genome sequence of bread wheat has been hindered by
the massive genome size (17 gigabases, which is 40 times the size of
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Please cite this article in press as: Brouns, F.J.P.H., et al., Does wheat make us fat and sick?, Journal of Cereal Science (2013), http://dx.doi.org/
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the rice genome and 5 times the size of the human genome) and the
hexaploid nature. However, a recent study identified 96,000 to
98,000 genes, many of which were assigned to the three genomes
(Brenchley et al., 2012). The large genome size, with a high content
of mobile elements, and the hexaploid nature have, however, also
resulted in high genome plasticity, which has facilitated rapid
adaptation and contributed greatly to the global success of the
wheat crop (Dubcovsky and Dvorak, 2007).
The wheat grain contains many hundreds of individual proteins, which may have structural, metabolic, protective or storage
functions (as reviewed by Shewry (2009)). They include the
gluten proteins, which are the major storage components and may
account for up to 80% of the total grain protein (Wrigley et al.,
1988). The protein composition of the grain is determined by
the genotype, but also strongly influenced by the environment
(climate and agronomy). For example, the contents of protective
proteins may be greater when the plant is subjected to heat or
drought stress while the total content of gluten proteins and the
proportions of different gluten protein components are influenced
by the availability of mineral nutrients (nitrogen and sulphur)
(Shewry, 2011).
Several popular nutritional plants, such as the Paleolithic diet
(CBS, 2012; Jönsson et al., 2006, 2005; Rose, 2011) and more
recently the proposal of the U.S. cardiologist W.R. Davis, in his
recent bestseller book, Wheat Belly (2011), have suggested that
(whole-)wheat consumption has adverse health effects, based on
different and controversial hypotheses. With this, they follow a
recent trend to pinpoint the cause of obesity to one specific type of
food or food component, rather than to overconsumption and
inactive lifestyle in general. Hence, following discussions on the
roles of fat, fructose, high fructose corn syrup and added sugar in
foods, it seems that it is now the turn of wheat to take the blame for
obesity. These discussions fail to take into account that obesity has a
multifactorial causation (Grundy, 1998; Keith et al., 2006).
For centuries, there have been populations who consume
wheat-based breads and other wheat products as the main source
of their energy intake, such as in Turkey, without indices of causing
weight gain. Moreover, the consumption of whole grain products,
which in the U.S. and Europe are mainly based on wheat, has been
shown to be associated with reduced risks of type 2 diabetes, cardiovascular disease, some types of cancer as well as a more
favourable weight management (Ye et al., 2012). It is also argued
that the current worldwide wheat production consists of “genetically modified” varieties, which contain new components that
cause adverse health effects. In reality, the presence of such new
components is not supported either by comparative studies of old
and recently bred types of wheat (Ward et al., 2008) or by analyses
of genomic sequences (Brenchley et al., 2012). Moreover, hard data
about adverse effects of wheat, consumed in baked, extruded, and
other processed foods, are not available, and there are no grounds
to advise the general public not to consume this common dietary
staple. Only individuals with a genetic predisposition for celiac
disease, or suffering from allergy or other forms of sensitivity to
gluten and other wheat proteins, will benefit from excluding wheat
and related cereals from their diet.
2. Materials and methods
To ensure the quality of the research, and to obtain transparent
and reproducible results, we made use of certain guidelines. In our
search strategy, we used several databases of controlled scientific
articles. All articles are referred to in the text and are available in
English. We discuss most the relevant articles and critically evaluate the data. We also consider the scientific evidence for possible
mechanisms based on recent literature.
3. Discussion
In a recent interview (CBS, 2012), the cardiologist W.R. Davis
discussed his recent bestselling book: Wheat Belly: Lose the Wheat,
Lose the Weight, and Find Your Path Back to Health (Davis, 2011). The
author stated that the wheat that we eat these days is “created by
genetic research in the 60s and 70s” leading to the inclusion of an
unnatural protein in our “modern wheat” called gliadin. When
coming to a conclusion, Davis explained that everybody is ‘susceptible’ to this gliadin protein as “gliadin binds into the opiate
receptors in your brain and in most people stimulates appetite,
such that we consume 440 more calories per day, 365 days per
year”.
In this light, it should be noted that gliadins are present in all
wheat lines and in related wild species (Goryunova et al., 2012). In
addition, seeds of certain ancient types of tetraploid wheat (e.g.;
Graziella Ra, Khorasan wheat/Kamut) have even greater amounts of
total gliadin than modern accessions (Colomba and Gregorini,
2012). Moreover, although the genetic engineering of wheat is
technically possible, it has only been used in research programs and
“GM wheat” has not been marketed or grown commercially in any
country. However, it could be argued that wheat has been “genetically modified” by plant breeding in the same way that other crops
and livestock species have been improved by selective breeding.
Because bread wheat arose in cultivation, rather than from
domestication of a wild species, it has probably been subjected to
selection for the whole of its 9000 year history, initially subconsciously by early farmers and later (over the past century) by the
application of scientific breeding. This has exploited variation
controlled by endogenous wheat genes, resulting particularly from
the high genome plasticity, with the limited use of related species
to transfer useful traits. The main traits selected have been high
yield, good resistance to pests and pathogens and good processing
properties (for bread, cookies, noodles and, in durum wheat, pasta).
There is no evidence that selective breeding has resulted in detrimental effects on the nutritional properties or health benefits of the
wheat grain, with the exception that the dilution of other components with starch occurs in modern high yielding lines (starch
comprising about 80% of the grain dry weight) (Shewry et al., 2011).
Selection for high protein content has been carried out for bread
making, with modern bread making varieties generally containing
about 1e2% more protein (on a grain dry weight basis) than varieties bred for livestock feed when grown under the same conditions (Monaghan et al., 2001; Snape et al., 1993). However, this
genetically determined difference in protein content is less than
can be achieved by application of nitrogen fertilizer (Godfrey et al.,
2010).
We consider that statements made in the book of Davis, as well
as in related interviews, cannot be substantiated based on published scientific studies. For the sake of brevity, we focus on four of
these arguments which we consider are most relevant to the
present discussion (other critical remarks are listed by Jones
(2012)), while further expanding on sound nutritional and cereal
science.
“The proliferation of wheat products parallels the increase in waist
size”
This statement implies that a correlation between two variables can be interpreted as a true causal relationship. It is
certainly true that the increase in wheat sales has a parallel with
an increase in obesity. However, there are also parallel increases
in the sales of cars, mobile phones, sports shoes and the average
speed of winners of the Tour de France. Similarly, a correlation
between the national consumption of chocolate and the number
of Nobel Prize winners has been reported (Messerli, 2012).
Please cite this article in press as: Brouns, F.J.P.H., et al., Does wheat make us fat and sick?, Journal of Cereal Science (2013), http://dx.doi.org/
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However, it is not valid to consider these correlations as causal
relationships, and in the examples listed above any such claim
would be ridiculed. Moreover, the proliferation of wheat products has a much longer history than the much more recent drastic
increases in occurrence of obesity, which has also occurred in
populations that eat little wheat, such as several Asian countries
(Yoon et al., 2006).
“The starch in wheat is different from that found in other
carbohydrate-rich foods such as bananas, potatoes and vegetables.
The amylopectin structure allows it to be very efficiently converted
to raise blood sugar” (undesirably).
The starch present in all plant tissues (including grains and
some vegetables and fruits) is a mixture of two polymers of
glucose, amylopectin and amylose. Amylose has a linear chemical
structure and is relatively slowly digested while amylopectin has
a more branched structure and is more rapidly digested. With
the exception of mutant lines, the ratio of the two polymers
varies little, being about 20e25% amylose and 70e75% amylopectin (Hoover and Zhou, 2003). Mutant lines include waxy
types, which comprise almost 100% amylopectin. Some waxy
lines are grown commercially (notably waxy rice) but not waxy
wheat. Furthermore, the ratio of amylose to amylopectin is
generally not the decisive factor for an effect on the blood sugar
level. It is also necessary to take into account other nutritional
factors such as prior meals, the content of fat, protein and fibre in
the meal as well as the matrix of the food product/meal. There
are also large differences between carbohydrate-rich foods that
easily fall apart in an aqueous environment, such as white bread,
and therefore are readily accessible to digestive enzymes and
foods that have a more solid and compact matrix, such as pasta,
macaroni and spaghetti which are digested less rapidly
(Juntunen et al., 2003). A study reported by Riccardi et al. (2003)
tested different foods to show that composition, preparation and
food matrix influence glycaemic response significantly, as
depicted in Fig. 1. However, the blood glucose response after
bread consumption was lower than the response after eating the
same amount of potatoes or white rice (reflected in the corresponding GI values (Foster-Powell et al., 2002)), which refute the
suggestion that starch from wheat generally leads to a higher
glycemic response.
“Whole-wheat bread has a Glycaemic Index (GI) of 72, which is
higher than that of sugar (GI ¼ 59)”
Fig. 1. 1 Composition, preparation and food matrix influence glycemic response
significantly (as studied by Riccardi et al. (2003)).
3
This statement may lead to the perception that, based on GI,
consuming sugar is better for your health than eating wheat. For
clarification, the GI is a measure of blood glucose response and is
expressed as an index comparing the consumption of a particular
food to the blood glucose response after intake of 50 g of glucose.
Since sugar (sucrose) consists of 50% glucose (GI ¼ 100) and 50%
fructose (GI ¼ 27), the GI of sugar, contrary to what many people
think, is relatively low. The internationally accepted average GI of
sucrose is not 59, as Davis indicates, but 67 (Foster-Powell et al.,
2002). This value is very close to the GI of white wheat bread,
which has a range of 69e73, with a mean of 70 (mean of 7 studies
(Foster-Powell et al., 2002). Furthermore, whole-wheat bread has a
slightly lower GI of 65.9 (mean of 8 Canadian studies (Foster-Powell
et al., 2002)). In fact, the amount of a particular carbohydrate eaten
x the GI, expressed as the glycaemic load, is much more meaningful
than the GI value alone. The statement above therefore misinterprets the background to the GI methodology (Brouns et al.,
2005) as well as the related digestive and metabolic mechanisms.
“Wheat opioids are so addictive that they cause people to be unable
to control their eating, and removal of wheat from the diet causes
withdrawal”.
There are no data available to substantiate this suggestion. The
gluten storage proteins of wheat belong to a broader class of
proteins with closely related forms being present in closely related
species (rye and barley) and less closely related forms in other
cereals (oats, millets, sorghum, corn and rice). Gluten proteins are
also present in the “primitive” wheat species discussed above:
einkorn, emmer and spelt. Gluten proteins are classically divided
into two fractions, the gliadins which are present as monomers
and the glutenins which are polymeric. Incomplete digestion of
gliadin has been shown to release a peptide, called gliadorphin,
that can induce opiate like effects, as demonstrated in laboratory
tests in rats that were infused with the intact peptide (Sun and
Cade, 2003). However, gliadorphin consists of seven amino acids
(Tyr-Pro-Gln-Pro-Gln-Pro-Phe) and, as such, cannot be absorbed
by the intestine. This is because the intestine peptide transporter
PepT1 transports only di- and triptides (Gilbert et al., 2008) and
transporters for larger peptides have not been identified. Gliadorphin is therefore not present in intact form in the human circulatory system and cannot reach and have an effect on the cells of
the central nervous system. In this respect, Davis extrapolates effects observed on cells in a laboratory setting to the in vivo situation in humans. There are no studies in which gliadorphin has been
shown to be absorbed in intact form by the intestine and no evidence that gliadin either stimulates appetite or induces addictionlike withdrawal effects. The author references a study to support
his argument in this respect, but the study referred to did not
include actual feeding of any food (Jones, 2012). By contrast,
Giacco, et al. (2011) and Koh-Banerjee et al. (2004) concluded that
regular consumption of whole grains was negatively correlated
with weight gain. These authors described 14 cross sectional
studies, most of which were performed in the USA, in which higher
intake of whole grains was correlated with a lower body mass
index (BMI). In addition, they presented three studies in which a
significantly lower waist circumference was noted. The argument
that refraining from consumption of wheat in the daily diet induces weight loss should also be interpreted in the light of the fact
that a very limited number of foods available in the market do not
contain wheat. This limited availability of wheat-free foods may
itself cause consumption monotony, leading to reduced overall
intake of food and energy. The latter will result in weight loss,
which will improve (type 2) insulin sensitivity and diabetic state, a
dieting-related phenomenon which occurs during virtually all
popular diet interventions.
Please cite this article in press as: Brouns, F.J.P.H., et al., Does wheat make us fat and sick?, Journal of Cereal Science (2013), http://dx.doi.org/
10.1016/j.jcs.2013.06.002
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4. Gluten sensitivity
Very recently, Soares et al. (2013) fed mice an ad libitum high-fat
diet to induce obesity. The mice were divided into a control group,
containing no gluten, and a group receiving 4.5% wheat gluten, for 8
weeks. The high-fat diet was composed of 25%, 61% and 15% of the
total energy from carbohydrate, fat and protein, respectively. As the
diet composition (excessive fat and low carbohydrate) was not
representative for the human diet, and there was no control group
in which the added gluten was exchanged for another isolated
protein type, to assure out that the effects observed were gluten
specific effect rather than a general protein content effect, we feel
that it is premature to follow the authors conclusion that gluten
exclusion helps in reducing body weight and that it can be a new
dietary approach to prevent the development of obesity and related
sickness in the general human population. Such statements on the
adverse effects of gluten-containing (whole-)wheat are diametrically opposite to the observations that the consumption of whole
grain and whole grain fibre significantly improves blood glucose
control, improves cholesterol levels, reduces blood pressure and
lowers the serum concentration of high sensitivity C-reactive protein, a marker of low grade inflammation (Gaskins et al., 2010;
Jenkins et al., 2007; Masters et al., 2010; Qi et al., 2006; Raninen
et al., 2011) These observations all indicate improvement in overweight related metabolic dysregulation (syndrome X) and have
been attributed largely to the fibre (b-glucan and arabinoxylan) and
phytochemicals (phenolics, sterols, tocols and vitamins) that are
concentrated in the aleurone layer of the bran (Brouns et al., 2011)
as well as present in the wheat germ fraction. These compounds, as
depicted in Fig. 2 (adapted from Barron et al. (2007), are thought to
exert synergistic effects on specific health-related metabolic processes (Fardet, 2010).
Recently, Björck, et al. (2011) summarized the findings of the
HEALTHGRAIN project supported by the European Commission
which included 26 academic research centres. They concluded that
in well-controlled studies a negative correlation was observed between the circulating levels of short-chain fatty acids (SCFA)
resulting from grain fibre fermentation in the colon and improved
insulin sensitivity and glucose homeostasis. As a consequence, insulin production at a certain carbohydrate load was favourably
reduced. This points to important effects of components that are
either not present, or only present in insignificant amounts in white
wheat flour, but are present in whole wheat and whole grain flour.
In this respect, it is also noteworthy that the digestion and metabolism of whole grain goods induces significantly different effects
on insulin-, incretin- and satiety hormone responses compared to
the consumption of refined (white flour based) wheat bread
(Juntunen et al., 2003).
Hauner et al. (2012), summarized the evidence on carbohydrate
intake and focused on the relation between wheat and nutritionrelated diseases. The authors conclude that the evidence
regarding the relevance of refined grain and whole-grain product
intake for the risk of obesity is judged as insufficient. Moreover,
they conclude that existing cohort studies show a possible relationship between whole-grain product intake and a reduced risk of
obesity, a probable relationship with a lower risk of diabetes (see
also: de Munter et al., 2007) and coronary heart disease, and a
convincing relationship with a reduced level of LDL cholesterol. In
addition, Aune, et al. (2011) concluded that the intake of dietary
fibre from cereals and other whole grains is associated with a
reduced risk of colorectal cancer.
Although the studies discussed above indicate that whole grain
consumption has health benefits, it should also be noted that part
of the population cannot tolerate wheat or other cereals containing
related proteins, particularly those suffering from celiac disease. CD
is a genetically predisposed condition (Catassi and Fasano, 2008;
Fasano and Catassi, 2001) and results from an autoimmune
response initiated by the binding of modified gluten peptides to Tcells of the immune system. The presented peptides are then
recognized by specific CD4þ T cells which release inflammatory
cytokines leading to damage of the gut villi. Individuals carrying
HLA-DQ2 or HLA-DQ8 as major genetic predisposition are affected,
representing w1% of the population. Rubio-Tapia et al. (2009)
concluded that the prevalence of CD in the United States was
0.71% (1 in 141), similar to that found in several European countries
(Mustalahti et al., 2010).
Very recently, gluten sensitivity has been defined as a new
etiologically heterogeneous syndrome in which environmental
factors may play a role in addition to that of food (Biesiekierski
et al., 2011; Carroccio et al., 2012a; Di Sabatino et al., 2012;
Pietzak, 2012). Other data shows that gluten sensitivity occurs in
approximately 30% of the people suffering from irritable bowel
syndrome (IBS). Given the prevalence of IBS in most countries, 10e
15% (in some countries >30%) (Carroccio et al., 2012b; Verdu et al.,
Fig. 2. Histological structure of wheat grain. Adapted from Barron et al. (2007) showing bioactive components which are related to the fiber fraction of wheat and are present in
whole wheat meal but absent in refined “white” flour.
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2009), and this number is probably an underestimate because
many sufferers are not diagnosed, our conservative estimate is that
gluten sensitivity affect at least 5e10% of the population.
It should be noted in this respect that gluten sensitivity is not
the same as wheat allergy (Battais et al., 2008), which occurs in
about 0.3e3.0% in adults and children. Wheat grain proteins are
involved in the three routes of sensitization: inhalation, contact and
ingestion. Depending on the route of allergen exposure and the
underlying immunologic mechanisms, wheat grain allergy can
appear as occupational asthma and rhinitis, contact urticaria or
classic food allergy affecting the skin, gut and/or respiratory tract.
Allergy may also appear as exercise-induced anaphylaxis. Apart
from gliadin and glutenin protein fractions, wheat allergy can be
caused by a large number of other wheat components (such as aamylase inhibitors, serpin (serine proteinase inhibitor), acylcoenzyme A oxidase, fructose-biphosphate aldolase and wheat
flour peroxidase) (Battais et al., 2008; Tatham and Shewry, 2008).
A recent study (Sapone et al., 2011) evaluated possible mechanisms underlying gluten sensitivity. Patients who were not
suffering from coeliac disease (proved by gut tissue biopsy analysis)
but were sensitive to gluten were exposed to a supervised 4-month
gluten or non-gluten diet. The main gastrointestinal symptoms of
the gluten-sensitive individuals were gas production, diarrhoea,
weight loss, and abdominal pain. In this study, the gluten-sensitive
individuals did, however, show decreased intestinal permeability
(as measured by urinary lactulose/mannitol test). In the only
available double-blind, randomized, placebo-controlled study
addressing wheat gluten sensitivity (Biesiekierski et al., 2010), a rechallenge trial was undertaken in patients with irritable bowel
syndrome in whom celiac disease was excluded and who were
symptomatically controlled on a gluten-free diet. Participants
received either gluten or placebo in the form of two bread slices
plus one muffin per day with a gluten-free diet for up to 6 weeks.
Symptoms were evaluated using a visual analogue scale and
markers of intestinal inflammation, injury, and immune-activation
were monitored. Although more intestinal distress symptoms were
reported in those consuming wheat gluten, there were no changes
in faecal lactoferrin, levels of celiac antibodies, high sensitive Creactive protein, or intestinal permeability. This highly controlled
study (Biesiekierski et al., 2010) clearly disproves the suggestion
that gluten protein in wheat and/or wheat germ agglutinin cause
adverse effects in individuals without celiac disease, thus giving no
reason to discourage the general population to consume wheat
containing products.
However, some gluten-containing products also contain relatively rapidly fermentable carbohydrates, such as oligofructose
and arabinoxylan. Exclusion of these and other fermentable oligo-,
di- and monosaccharides as well as polyols; (also referred to as
“FODMAPs”) from the diet has been reported to reduce intestinal
distress to similar extents as gluten free diets (Barrett and
Gibson, 2012). It is therefore still unclear whether gluten proteins or other factors are involved in the aetiology of gluten
sensitivity in non-celiac patients (Biesiekierski et al., 2011).
The very recent studies of Schuppan et al. (2012) and Junker
et al. (2012) on “cereal triggers of innate immune activation”
describe the role of wheat amylase-trypsin inhibitors (ATIs),
which probably confer defence against pests and parasites by
inhibiting their digestive enzymes. The authors state that, based
on the review of Ryan (1990), the breeding of high yielding and
highly pest-resistant varieties of wheat has automatically lead to
the selection of types that have a high content of ATIs. According
to Altenbach et al. (2011), the ATIs are accumulated to sufficiently
high levels in the grain to also function as storage proteins. These
ATIs appear to largely resist intestinal degradation in humans
and stimulate mucosal cytokine release after feeding in vivo.
5
Preliminary studies showed that neither gliadin which had been
digested in vitro with trypsin and pepsin nor the celiac-active
peptide 31e43 from a-gliadin elicited innate immune responses
in intestinal epithelial cells. The pepsin-trypsin digested gliadin
(but not p31e43) did strongly activate inflammatory responses
but this activity was due to the presence of contaminating ATIs.
These findings identify cereal ATIs as novel contributors to celiac
disease. Moreover, the authors suggest that ATIs may fuel inflammation and immune reactions in other intestinal and even nonintestinal immune disorders (Junker et al., 2012). This clearly
warrants further research to unravel oral tolerance and gut disease
related mechanisms. However, the existence of many anecdotal
patient reports should not be ignored due to lack of scientific data
and evidence, but used as a basis for well-designed studies and
with more specific biomarkers.
In this respect, some medical doctors advise those who suffer
from physical complaints that cannot be explained on the basis of
routine medical testing (no physical cause can be established) to
request a gluten sensitivity test and/or to refrain for several weeks
from consuming gluten-containing foods to see whether their
symptoms (such as sensitive intestinal system, gastrointestinal
distress, bloating, rumbling, colic, chronic fatigue, poor concentration, ADHD, frequent headache, migraine, repeating episodes of
loose stools of diarrhoea and arthritis) disappear.
5. Conclusion
Although the adverse effects of wheat on some individuals
should not be ignored, five major recent scientific reviews addressing the impact of cereal consumption on health and disease
concluded that the consumption of whole grains, of which globally
most widely consumed is wheat, generally exerts positive effects on
health, thus recommending increased intake of whole grain for the
general public, in exchange for refined foods (Björck et al., 2011;
Fardet, 2010; Hauner et al., 2012; Jonnalagadda et al., 2011).
Wheat-containing foods prepared in customary ways and eaten
in recommended amounts have been associated with numerous
health benefits. In particular, the regular consumption of wholegrain products has been shown to be associated with significant
reductions in risks for type 2 diabetes and heart disease and more
favourable long term weight management. These findings are
supported by the outcome of a recent cohort, where it was
observed that individuals who consumed recommended amounts
of (whole)-wheat had the least amount of visceral fat accumulation
(Molenaar et al., 2009). Arguments that the currently consumed
wheat has been genetically modified resulting in adverse effects on
body weight and illnesses cannot be substantiated. In particular,
populations in some countries have obtained the major part of their
daily energy intake from wheat-based foods for many years, such as
Turkey, without reporting any detrimental effects on body weight
or chronic disease. In line with this is the evidence that grains and
grasses have already been consumed and processed throughout
Europe during the Mid-Upper Palaeolithic era (Revedin et al., 2010).
However, individuals who have a genetic predisposition for
developing celiac disease or who are sensitive to gluten and/or
allergic to wheat will benefit from avoiding wheat and other cereals
containing related proteins, including primitive wheats (einkorn,
emma, spelt), rye and barley. It is important that the food industry
should be developing a much wider spectrum of foods for this
section of the population, based on crops that do not contain proteins related to gluten, such as teff, amaranth, oat, quinoa, chia. The
recent development of commercial high yielding varieties of oats
(which are considered safe for those suffering from intolerance to
gluten) is an important step in this respect. Further research and
development on allergy and intolerance to wheat is also warranted,
Please cite this article in press as: Brouns, F.J.P.H., et al., Does wheat make us fat and sick?, Journal of Cereal Science (2013), http://dx.doi.org/
10.1016/j.jcs.2013.06.002
6
F.J.P.H. Brouns et al. / Journal of Cereal Science xxx (2013) 1e7
with various strategies being proposed to reduce exposure to
gluten (Gilissen et al., 2012; Shewry et al., 2012). These include the
reduction of (celiac) immunogenic epitopes in existing foods/grains
that contain gluten, the production of guaranteed safe, gluten-free
foods for patients with celiac disease and gluten intolerance and
increasing the production of foods based on crops that do not
contain proteins related to gluten. Since about 1% of the current
population of Europe and the U.S. population suffers from celiac
disease and probably 5e10% from gluten sensitivity (due to difficulties to diagnose this condition, the real number may even be
higher), these strategies will have both global economic and public
health impacts.
Conflict of interest
The authors declare to have no conflict of interest.
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